Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An enzyme immuno assay kit has been developed to detect anti-HIV antibody in urine. In order to examine the clinical utility of the kit, 1333 urine samples were assayed. These samples consisted of 233 urine samples from HIV infected patients, 472 samples from HIV uninfected patients including 203 samples from patients with urogenital diseases, and 628 samples from normal subjects. Anti-HIV antibodies were detected in all the urine samples from HIV infected patients, and the diagnostic sensitivity for HIV infection was 100% with no false negative cases. A variety of anti-HIV antibody titers were found in the urine samples from HIV infected patients. However, no significant differences were found in the distribution patterns of urinary anti-HIV antibody titers among AC, ARC and AIDS patients. False positives were determined in only five samples in 628 healthy subjects (0.8%), one in 19 patients with hepatitis (5.3%), one in 45 patients with hemophilia (2.2%) and two in 105 pregnant women (1.9%). The antibody titers of all the false positive samples in these groups were less than the cut-off index multiplied by two. However, relatively high positive rates were demonstrated in the samples from urogenital diseases (11.8%), diabetes mellitus (20.0%) and auto-immune diseases (7.3%). False positive results were found to be directly correlated to the protein concentration of urinary protein, especially the immunoglobulin concentration in urine. The assay system was also evaluated by various reproducibility tests performed by different operators at different laboratories. The test results were satisfactory.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical usefulness of urinary anti HIV antibody test--a large scale study from 11 institutes in Japan]. 774 30

Hepatitis C viruses (HCV) present in 110 Italian patients were characterized by genotype-specific PCRs. Among the 65 cases of community-acquired hepatitis, HCV genotype II was dominant (60%), followed by genotypes IV (15%), III (11%), and I (3%). Among the 45 hemophilia-associated cases, the distribution of the four HCV genotypes was markedly different: genotype I was the most prevalent (61%), followed by genotypes II (25%), III (4%), and IV (2%). Double infections were observed in eight patients. Two HCV remained unclassified. For the 45 community-acquired cases from which a liver biopsy was available, genotype II was associated with more severe liver damage than the other types.
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PMID:Prevalence of hepatitis C virus genotypes in Italy. 812 88

This report reviews the natural history of hemophilia and the development of concentrates as the preferred form of treatment and discusses the nature of immune defect in persons with hemophilia. It examines the risk of hepatitis and effect of HIV infection on treatment protocols, and it surveys the status of the safety of modern concentrates and what we have to look forward to in the future.
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PMID:HIV infection in hemophilia. 822 5

Molecular biology techniques are now a vital part of hepatitis virology, with a central role in studies of diagnosis, epidemiology, virology, pathogenesis, and natural history of infection. Cloning of the genome of hepatitis E virus has allowed its tentative classification as a calici- or related virus, and is the first step toward the development of a vaccine. Long-term implications of hepatitis C for groups such as children with hemophilia, thalassemia, and even leukemia can be better understood by comparison of virus load measured by molecular amplification of the plasma viral RNA with the serologic and clinical status of the respective cohorts of children. A new vaccine for hepatitis A has been licensed in several European countries, and recent experience with severe hepatitis in infants after unexpected transmission of hepatitis B from anti-hepatitis B e positive mothers reemphasizes the value of universal hepatitis B immunization programs. Mother-to-infant transmission of hepatitis C virus has now been well documented, but there are still insufficient data on the dynamics of this, particularly in the absence of passive immunoprophylaxis or a vaccine, to permit recommendations regarding the management of individual pregnancies or deliveries. There is especially too little information to suggest whether breast feeding may be an important mechanism for transmission.
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PMID:Hepatitis viruses and protection against infection in children. 837 24

Post ESWL haemorragic complications are frequent and most patients experience temporary haematuria and focal intrarenal bleeding or perirenal haematoma are detected by NMR or US imaging. By tradition coagulation troubles have been a contraindication for ESWL but literature describes cases of coagulopathic patients treated with ESWL. From January 1992 to July 1993, 4 of our patients with severe haemostatis troubles (severe haemophilia A in two cases, acquired deficit of coagulation factors and mild thrombocytopenia secondary to post-necrotic hepatitis in 1 case and Glanzmann's thrombasthenia in 1 case) underwent ESWL using Dornier HM3 mod. or MPL 9000. An extensive haematological and clinical evaluation pre and post-ESWL with an adequate haematological prophylaxis (transfusion of blood derivatives) has been performed depending on the coagulation disorder. In our patients we did not observe any haemorragic complication and we propose a reappraisal of the contraindications of ESWL in subjects with coagulation disorders: careful evaluation of haemorragic risk factors, by suitable correction measures and close clinical and instrumental monitoring, allows a reduction of the risk of haemorragic complications in coagulopathic patients who undergo ESWL treatment.
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PMID:[Extracorporeal lithotripsy in patients with acquired or congenital coagulopathies]. 858 Sep 83

Liver biopsy (n = 35) and autopsy (n = 71) specimens from HIV infected HCV-positive and HCV-negative haemophiliacs and non-haemophiliacs and liver biopsies (n = 33) from HIV-negative HCV-infected haemophiliacs and non-haemophiliacs were studied by histo- and immunohistochemistry to investigate the influence of HIV-coinfection on chronic C hepatitis (> 10 years duration). Almost all HIV-infected patients had a CD4 cell counts < 200/microns3. In biopsies and autopsies HCV-infection lead to stronger portal, periportal and lobular inflammatory changes independent from HIV-infection and haemophilia. However, HIV-infected patients with HCV-coinfection showed much more granulocytic infiltrates, particularly in the small bile ducts. In biopsies and autopsies HCV infection was associated with a stronger (centrilobular) fibrosis, particularly in HIV-positive haemophiliacs, and significantly stronger compared to HCV-negative patients. In the autopsy group half of the HIV-infected and HCV-positive haemophiliacs (n = 20) had developed posthepatitic liver cirrhosis due to C hepatitis, contrasted by two liver cirrhosis in HCV-infected non-haemophiliacs (n = 6) due to chronic B and C hepatitis and chronic alcohol abuse; no liver cirrhosis was observed in HIV-positive HCV-negative non-haemophiliacs (n = 45). Cholestasis and mild granulocytic cholangiolitis was a predominant feature in HIV/HCV-coinfection and similar distributed in haemophiliacs and non-haemophiliacs. The findings are suggestive that HIV-coinfection aggravates the course of a preceding hepatitis C virus infection, by a more granulocytic inflammatory infiltrate, stronger (centrilobular) fibrosis followed by a high incidence of posthepatitic cirrhosis--particularly in multitransfused haemophiliacs--and by cholestatic hepatopathy.
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PMID:[Hepatitis and posthepatic cirrhosis in AIDS]. 860 Jun 88

Hepatitis C virus (HCV) infection is the major cause of chronic liver disease in individuals with haemophilia. A wide spectrum of disease severity is found in this group, ranging from mild hepatitis to cirrhosis. We have studied a cohort of 87 anti-HCV positive haemophiliacs who have been infected with HCV for 10-25 years and assessed the relative value of invasive and non-invasive methods of evaluating liver disease. The severity of liver disease was assessed using ultrasound scan (n = 77), upper GI endoscopy (n = 50), laparoscopic liver inspection (n = 33) and liver biopsy (n = 22). Invasive investigations were performed without any significant bleeding complications. Evidence of severe liver disease was found in approximately 25% of patients. There was agreement between the severity of liver histology and the information derived from the laparoscopic liver inspection, endoscopy and ultrasound in 86%. Co-infection with HIV was significantly associated with more severe liver disease (P = 0.006). This study provides further evidence that liver disease is emerging as a major complication in haemophiliacs and severe liver disease is more common in those co-infected with HIV. We have shown the potential value of laparoscopic liver inspection, in combination with endoscopy and ultrasound, in staging the extent of liver disease, and suggest that most patients may be managed without resorting to liver biopsy.
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PMID:Investigation of chronic hepatitis C infection in individuals with haemophilia: assessment of invasive and non-invasive methods. 875 28

Many patients with haemophilia are infected with viruses, due to treatment with blood products--particularly from large pool clotting factor concentrates before 1985. AIDS in haemophilic patients was first described in 1982 and it has significantly reduced the life expectancy of these patients. Although no new sero-conversions have occurred since 1986, management of HIV in haemophilia remains a clinical challenge. Transfusion-associated hepatitis was recognized in 1943, and it is now an important complication of haemophilia treatment. Vaccination against HAV is recommended. Intensively-treated older haemophilic patients usually have serological evidence of HBV infection. HBV transmission has been stopped, but hepatitis B vaccination is still practised, because HDV requires HBV for propagation. Many patients are infected with HCV: before 1985 almost all patients who received clotting factor concentrate developed non-A, non-B hepatitis, now recognized as HCV. Treatment strategies are being developed for HCV in haemophilic patients. Parvo virus can be transmitted by clotting factor concentrate; it is very resistant to sterilization processes, transmission causing severe illness even in immuno-competent individuals. New blood-borne viruses responsible for sero-negative hepatitis include: GBV-A, B and C, and HGV. Although there is no link between CJD and haemophilia, there is concern about possible blood product transmission.
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PMID:Transfusion-transmitted disease. 880 May 11

The aftermath of the HIV catastrophe and hepatitis virus transmission to hemophiliacs has been characterized by continuous efforts to improve the purity of factor VIII and factor IX concentrates, increasing sophistication of the virucidal methods used, and the introduction of recombinant factor VIII. The cost of hemophilia care is substantial and there is a large price difference between products depending on their purity; generally, the purer the concentrate, the higher the price. The use of expensive highly purified concentrates may be questioned if these products are not superior in terms of safety, efficacy or convenience. The properties of concentrates used in hemophilia care are discussed in this review, as are their safety and side effects. The available data do not clearly reveal any clinical difference between factor VIII concentrates, although the highly purified products may be of theoretical benefit. With regard to factor IX, purified products do not seem to carry any risk of the well-known thromboembolic complications which occur in certain situations after treatment with prothrombin complex concentrates.
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PMID:Why prescribe highly purified factor VIII and IX concentrates? 880 65

RNA of a putative non-A, -B, -C, -D, or -E hepatitis virus named GB virus C (GBV-C) was detected by reverse transcription-polymerase chain reaction with primers deduced from the 5' untranslated region in 15 (24%) of 63 men with hemophilia in Japan at a frequency higher (P < .001) than that in 2 (0.6%) of 337 controls. By phylogenetic analysis, GBV-C isolates from some patients were similar in sequence, indicating infection with closely related strains, and those from certain patients resembled sequences reported from foreign countries. All patients were infected with hepatitis C virus, and genotypes that are rare in Japan were detected in 36 (57%) of them. These results indicate that patients with hemophilia in Japan would be at increased risk for infection with GBV-C and hepatitis C virus, some of which would have been transmitted via imported coagulation factor concentrates in the past.
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PMID:Molecular investigation of GB virus C infection in hemophiliacs in Japan. 920 72


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